Imatinib treatment of CML cells quickly causes cell cycle arrest at G0/G1 [39] where NHEJ operates predominantly [40], but the treatment stress elicits a new wave of modification of DNA repair in arrested cells by altering LSD1 and SIRT1 interaction with KU70 and likely changing repair kinetics and fidelity, which has crucial impact on mutation acquisition. This evidence concerns the gene KDM1A and chronic myelogenous leukemia, BCR-ABL1 positive.